Effect of ORF7 of SARS-CoV-2 on the Chemotaxis of Monocytes and Neutrophils In Vitro

Abstract

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently the most significant public health threat worldwide. Patients with severe COVID-19 usually have pneumonia concomitant with local inflammation and sometimes a cytokine storm. Specific components of the SARS-CoV-2 virus trigger lung inflammation, and recruitment of immune cells to the lungs exacerbates this process, although much remains unknown about the pathogenesis of COVID-19. Our study of lung type II pneumocyte cells (A549) demonstrated that ORF7, an open reading frame (ORF) in the genome of SARS-CoV-2, induced the production of CCL2, a chemokine that promotes the chemotaxis of monocytes, and decreased the expression of IL-8, a chemokine that recruits neutrophils. A549 cells also had an increased level of IL-6. The results of our chemotaxis Transwell assay suggested that ORF7 augmented monocyte infiltration and reduced the number of neutrophils. We conclude that the ORF7 of SARS-CoV-2 may have specific effects on the immunological changes in tissues after infection. These results suggest that the functions of other ORFs of SARS-CoV-2 should also be comprehensively examined.

Exploration of the Link Between COVID-19 and Alcoholic Hepatitis from the Perspective of Bioinformatics and Systems Biology

“…Studies on lung type II lung cells (A549) have shown that the open reading framework (ORF) 7 in the genome of the new coronavirus induces the production of the chemokine CCL2 that promotes the chemotaxis of monocytes and reduces the expression of the chemokine IL-8, which recruits neutrophils. ORF7 increases monocytes infiltration, reduces the number of neutrophils, and may have a specific effect on immunological changes in tissues after infection(35). Similarly, for the results of a study of AH suggest that in primary biliary cirrhosis (PBC), there is a functional monocyte disturbance which seems to be primary and may arise at the cellular level and is the way that SARS-CoV-2 could anabasis(36).…”